Yonsei University · Medicine
Professor Hyun Sil Kim's research lab focuses on the molecular mechanisms underlying cancer metabolism, particularly the role of metabolic reprogramming in tumor progression and therapeutic resistance. The lab investigates key regulators such as Snail (SNAI1) in modulating catabolic pathways like fatty acid oxidation and glycolysis, with a strong emphasis on how these processes support cancer cell survival under stress. Additionally, the lab explores the pathophysiology of fibrotic diseases, especially in salivary glands, by examining the TGF-β signaling pathway and its potential as a therapeutic target. The integration of immunology, cancer metabolism, and fibrosis mechanisms defines the lab’s interdisciplinary approach to understanding disease mechanisms and identifying novel therapeutic strategies.
Figures are computed from collected data and may differ slightly.
CD1d is a major histocompatibility complex class I-like molecule that exhibits a distinct antigen processing pathway that functions in the presentation of hydrophobic antigens to T cells. CD1d has been previously shown to be expressed on the cell surface of human intestinal epithelial cell lines in vivo and a transfected cell line in vitro independently of beta2-microglobulin (beta2m). To define the relationship between CD1d and beta2m and characterize the biochemical structure of CD1d in the ab
Fibrosis is presented in various physiologic and pathologic conditions of the salivary gland. Transforming growth factor beta (TGF-β) pathway has a pivotal role in the pathogenesis of fibrosis in several organs, including the salivary glands. Among the TGF-β superfamily members, TGF-β1 and 2 are pro-fibrotic ligands, whereas TGF-β3 and some bone morphogenetic proteins (BMPs) are anti-fibrotic ligands. TGF-β1 is thought to be associated with the pro-fibrotic pathogenesis of sialadenitis, post-rad
Despite the importance of mitochondrial fatty acid oxidation (FAO) in cancer metabolism, the biological mechanisms responsible for the FAO in cancer and therapeutic intervention based on catabolic metabolism are not well defined. In this study, we observe that Snail (SNAI1), a key transcriptional repressor of epithelial-mesenchymal transition, enhances catabolic FAO, allowing pro-survival of breast cancer cells in a starved environment. Mechanistically, Snail suppresses mitochondrial ACC2 (ACACB
The purpose of this study was to investigate the current status of international marriage migrant women living in Daegu and Kyungpook area, and to identify the impacts of social support and life satisfaction on their depression in this population. Methods: Research objectives were accomplished by conducting an anonymous questionnaire survey with 173 international marriage migrant women. Data were analyzed using descriptive analysis, Pearson correlation coefficients and stepwise multiple regressi
In this paper, the sound transmission loss (STL) of thin double plates with an air cavity between them in a rigid duct is considered using an analytical approach. The vibration motion of the plate and sound pressure field are expanded in terms of an infinite series of the modal functions. Under the plane wave condition, a low frequency solution is derived by including the first few symmetric modes. It is determined that the peak frequencies of the double plates coincide with those of each single
Efficient catabolic metabolism of adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) is essentially required for cancer cell survival, especially in metastatic cancer progression. Epithelial-mesenchymal transition (EMT) plays an important role in metabolic rewiring of cancer cells as well as in phenotypic conversion and therapeutic resistance. Snail (SNAI1), a well-known inducer of cancer EMT, is critical in providing ATP and NADPH via suppression of sev
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